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Molecular mechanisms of gasdermin D pore-forming activity

NATURE IMMUNOLOGY (2023)

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Zihao Yuan et al.

Summary: This study investigates the origin, evolution, and function of GSDM in different organisms. GSDM was found to emerge in Placozoa and be absent in most invertebrates. Three types of GSDME were identified in fish, with distinct evolutionary separation. GSDMEc is closely related to GSDMA and possibly its prototype.

FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY (2022)

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The Gasdermin D N-terminal fragment acts as a negative feedback system to inhibit inflammasome-mediated activation of Caspase-1/11

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A bacterial phospholipid phosphatase inhibits host pyroptosis by hijacking ubiquitin

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NINJ1 mediates plasma membrane rupture during lytic cell death

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Intracellular immune sensing promotes inflammation via gasdermin D-driven release of a lectin alarmin

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The metabolite α-KG induces GSDMC-dependent pyroptosis through death receptor 6-activated caspase-8

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Summary: Pyroptosis is induced by alpha-ketoglutarate through caspase-8-mediated cleavage of GSDMC. This process involves elevation of ROS levels leading to oxidation of DR6 and endocytosis, ultimately resulting in pyroptosis. The acidic environment and production of L-2HG play a crucial role in enhancing the efficiency of alpha-KG-induced pyroptosis in cancer cells.

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Virus-mediated inactivation of anti-apoptotic Bcl-2 family members promotes Gasdermin-E-dependent pyroptosis in barrier epithelial cells

Megan H. Orzalli et al.

Summary: During viral infection, inhibition of protein synthesis triggers pyroptosis in human keratinocytes, leading to the release of inflammatory cytokines. MCL-1 and BCL-xL act as sensors of translation shutdown, contributing to antiviral defense by inhibiting virus replication.

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NLRP3 inflammasome activation triggers gasdermin D-independent inflammation

Chun Wang et al.

Summary: NLRP3 inflammasome, upon sensing pathogen products or sterile danger signals, processes pro-IL-1 beta and pro-IL-18 into bioactive cytokines IL-1 beta and IL-18 with the involvement of GSDMD. However, research shows that even in the absence of GSDMD, NLRP3 activation can still independently trigger inflammatory responses.

SCIENCE IMMUNOLOGY (2021)

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Gasdermin D pore structure reveals preferential release of mature interleukin-1

Shiyu Xia et al.

Summary: Inflammasomes activate caspase-1 to cleave GSDMD and generate mature cytokines like IL-1 beta and IL-18, which are released through pores formed by GSDMD. The GSDMD pore mediates IL-1 release by electrostatic filtering, favoring the passage of mature cytokines over their precursors.

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Select hyperactivating NLRP3 ligands enhance the TH1-and TH17-inducing potential of human type 2 conventional dendritic cells

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Summary: The conventional type 2 DC (cDC2) subset has been found to be transcriptionally and functionally poised for inflammasome formation and response without pyroptosis when stimulated with relatively weak inflammasome activators, leading to the induction of prominent T helper type 1 (T(H)1) and T(H)17 responses. These findings suggest that the human cDC2 subpopulation could be a prime target for the treatment of inflammasome-dependent inflammatory diseases and provide insights for new approaches in adjuvant and vaccine development.

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Gasdermin D mediates the maturation and release of IL-1α downstream of inflammasomes

Kohsuke Tsuchiya et al.

Summary: This study demonstrates that GSDMD is essential for the rapid maturation of IL-1α by nonparticulate inflammasome activators. Ablation of GSDMD prevents the maturation of IL-1α but not IL-1β. The maturation of IL-1α induced by inflammasomes relies on extracellular calcium and calpains, which are induced in a GSDMD-dependent manner.

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Gasdermin E permits interleukin-1 beta release in distinct sublytic and pyroptotic phases

Bowen Zhou et al.

Summary: Gasdermin E (GSDME) functions as an independent conduit for interleukin-1b (IL-1b) release in cellular inflammasome activation, regardless of its cell death ability. Our study reveals that both NLRP3 and NLRP1 inflammasomes depend on both gasdermins for IL-1b processing and release, apart from their ability to induce cell lysis.

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Article Biochemistry & Molecular Biology

Control of gasdermin D oligomerization and pyroptosis by the Ragulator-Rag-mTORC1 pathway

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Summary: The Ragulator-Rag complex is found to be necessary for GSDMD pore formation and pyroptosis in macrophages, promoting GSDMD oligomerization on the plasma membrane. Defects in GSDMD oligomerization and pore formation can be rescued by mitochondrial poisons that stimulate ROS production, and ROS modulation impacts the ability of inflammasome pathways to promote pore formation downstream of GSDMD cleavage.

CELL (2021)

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Pathogenic ubiquitination of GSDMB inhibits NK cell bactericidal functions

Justin M. Hansen et al.

Summary: GSDMB is targeted and destroyed by the IpaH7.8 effector protein secreted by Shigella flexneri, protecting the bacterium from natural killer cells. Unlike other gasdermin family members, GSDMB exhibits direct microbiocidal activity by recognizing phospholipids found on Gram-negative bacterial membranes.

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Article Microbiology

Shigella ubiquitin ligase IpaH7.8 targets gasdermin D for degradation to prevent pyroptosis and enable infection

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Summary: The study reveals the mechanism by which IpaH7.8 from Shigella ubiquitinates human GSDMD and targets it for proteasomal degradation, contributing to the bacterium's impact on humans rather than mice.

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Gasdermins mediate cellular release of mitochondrial DNA during pyroptosis and apoptosis

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Summary: Gasdermin processing is necessary for mitochondrial DNA release during pyroptosis and apoptosis, and it plays a critical role in facilitating the release of mitochondrial DNA as a damage-associated molecular pattern.

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Summary: This article provides an update on the role of inflammasomes in SARS-CoV-2 infection and COVID-19, discussing their activation and contribution to the overactive inflammatory response in severe cases. Efforts are being made to target inflammasomes therapeutically. Severe COVID-19 is characterized by dysregulated cytokine release, pneumonia, and acute respiratory distress syndrome, with ongoing clinical efforts to suppress inflammation for prevention and treatment.

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mtDNA Activates cGAS Signaling and Suppresses the YAP-Mediated Endothelial Cell Proliferation Program to Promote Inflammatory Injury

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Granzyme A from cytotoxic lymphocytes cleaves GSDMB to trigger pyroptosis in target cells

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Chemotherapy-induced pyroptosis is mediated by BAK/BAX-caspase-3-GSDME pathway and inhibited by 2-bromopalmitate

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